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RPA1 Remodels Liver Chromatin Architecture to Maintain Lipid Metabolic Homeostasis

ABSTRACT: RPA1 Remodels Liver Chromatin Architecture to Maintain Lipid Metabolic Homeostasis

PROVIDER: PRJNA510120 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8321190.fastq.gz	Fastqsanger.gz
	SRR8321191.fastq.gz	Fastqsanger.gz
	SRR8321192_1.fastq.gz	Fastqsanger.gz
	SRR8321192_2.fastq.gz	Fastqsanger.gz
	SRR8321193_1.fastq.gz	Fastqsanger.gz

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RPA1 Remodels Liver Chromatin Architecture to Maintain Lipid Metabolic Homeostasis

Project description:Replication protein A(RPA), a ssDNA binding protein complex, participates in DNA replication, recombination and damage repair, but its physiological function remains elusive. Here, we show that heterozygous Rpa1 knockout mice were developmentally normal, but hypersensitive to ageing and high-fat-diet (HFD) induced hepatic steatosis. Liver specific deletion of Rpa1 leads to impaired lipid beta-oxidation, hepatic steatosis and subsequently hepatocellular carcinoma (HCC). Assays for RNA-seq, pull-down and transposase-accessible chromatin sequencing (ATAC-seq) reveal that RPA1 is required for transcription of a subgroup of lipid metabolic genes via altering chromatin accessibility landscape. Thus, our results suggest that RPA1 is a critical regulator of gene transcription and chromatin remodeling, linking a guardian of genome stability to lipid metabolic homeostasis.

2024-12-21 | GSE123890 | GEO

RPA1 controls chromatin architecture and maintains lipid metabolic homeostasis

Project description:Replication protein A1 (RPA1) is a single-stranded DNA binding protein that is known to participate in DNA replication, recombination and damage repair. However, little is known about RPA1’s role in controlling chromatin architecture and gene transcription. Further, physiological functions of RPA1 in mouse tissues still remain exclusive. Here we show that Rpa1 heterozygous mice developed age-depended fatty liver disease and are more susceptible to hepatic steatosis in response to high-fat diet. Liver specific deletion of Rpa1 impairs fatty acid oxidation, leading to hepatic steatosis and high incidence of hepatocellular carcinoma. Transcriptome analysis identified down-regulation of fatty acid oxidation related genes. Cleavage Under Targets and Tagmentation (CUT&Tag) and Assay for transposase-accessible chromatin using sequencing (ATAC-seq) revealed that RPA1 binds and regulates chromatin accessibility in regulatory regions of a group of genes involved in lipid metabolism in liver. Further, down-regulation of RPA1 was found in patients with fatty liver disease. Thus, our results not only established that RPA1 is critical controller of chromatin architecture and regulator of gene transcription, but also provided new insights into the epigenetic mechanism of fatty liver disease, which could inform future therapy.

2022-07-18 | GSE158575 | GEO

The role of RPA1 in T cell

Project description:As a single strand DNA binding protein, RPA1 participates various cellular processes including DNA replication and DNA repair.However, the role of RPA1 in T cell is largely unknown. We generate a mice model in which RPA1 was specifically deleted in T cell. Through single cell RNA sequencing, we reveal the immune landscape in RPA1 conditional knockout mice.

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The role of RPA1 in T cells [thymus]

Project description:As a single strand DNA binding protein, RPA1 participates in various cellular processes including DNA replication and DNA repair. However, the role of RPA1 in T cells is largely unknown. We generated a mouse model in which RPA1 was specifically deleted in T cells. Through single cell RNA sequencing, we reveal the immune landscape in RPA1 conditional knockout mice.

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CDKN2A remodels lipid metabolism to prime glioblastoma for ferroptosis

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Serratia marcescens strain:RPA1

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Sensory experience remodels genome architecture in neural circuit to drive motor learning

Project description:Neuronal activity-dependent transcription couples sensory experience to adaptive responses of the brain including learning and memory. Mechanisms of activity-dependent gene expression including alterations of the epigenome have been characterized. However, the fundamental question of whether and how sensory experience remodels chromatin architecture in the adult brain in vivo to induce neural code transformations and learning and memory remains to be addressed. Here, in vivo calcium imaging, optogenetics, and pharmacological approaches reveal that granule neuron activation in the anterior dorsal cerebellar vermis (ADCV) plays a crucial role in a novel delay tactile startle learning paradigm in mice. Strikingly, using large-scale transcriptome and chromatin profiling, we have discovered that activation of the motor learning-linked granule neuron circuit reorganizes neuronal chromatin including through long-distance enhancer-promoter and transcriptionally active compartment interactions to orchestrate distinct granule neuron gene expression modules. Conditional CRISPR knockout of the chromatin architecture regulator Cohesin in ADCV granule neurons in adult mice disrupts activity-dependent transcription and motor learning. These findings define how sensory experience patterns chromatin architecture and neural circuit coding in the brain to drive motor learning.

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